DESCRIPTION A major cause of neonatal morbidity is pre-term birth. Among the factors associated with this observation are bacterial vaginosis and urinary tract infections, which can result in local or systemic endotoxin exposure, and are risk factors for prematurity and low birth weight infants. The principal investigator suggests that endotoxin and the inflammatory mediators it stimulates may represent a link between urogenital infections and prematurity. Using a well characterized animal model, the preimplantation mouse embryo, the principal investigator will analyze the impact of endotoxin (lipopolysaccharide) on this system. Two specific aims are proposed. The first will test the hypothesis that sublethal doses of endotoxin initiate an oxidative stress response in the preimplantation embryo. The expression of several genes known to react to oxidative stress, and others which produce protective proteins against oxidative stress will be analyzed. The second will test the hypothesis that exposure of the preimplantation embryo in vitro to sublethal doses of endotoxin will produce an increase in growth and developmental abnormalities in vivo following transfer to foster mothers and analyzing the results on 7.5 days of gestation.